PubMed Health⌕ Search

Biomedical subjects

K Hodson

Publications and source records attributed to K Hodson.

6 recordsLinked to original sources
PubMed1997

Are coagulation studies on blood sampled from arterial lines valid?

Coagulation tests were performed on two venous blood samples and two blood samples from arterial lines taken from 79 patients on an intensive care unit. For the first arterial sample the discard volume was 4.5 ml and for the second arterial sample the discard volume was 16 ml. From each pair of venous samples a mean venous coagulation value was calculated. There were statistically significant differences between arterial and venous results and between the two arterial samples for activated partial thromboplastin time and thrombin time assays but not for prothrombin time, reptilase time and fibrinogen assays. However, these differences were sufficiently small to be of little clinical significance. The bias for the difference in activated partial thromboplastin time values between the first arterial sample and the venous sample was +1.24 s (limits of agreement: -4.39 to +6.87 s) and between the second arterial sample and the venous sample the bias was +0.89 s (limits of agreement: -3.25 to +5.03 s). Only 3.8% of first arterial samples and 1.3% of second arterial samples produced activated partial thromboplastin time values that were more than 10% longer than the corresponding venous values. No heparin was detectable in these arterial samples using a heparin assay (< 0.02 iu.ml-1). The differences between arterial and venous activated partial thromboplastin times were slightly but not significantly greater in subgroups of patients with moderately or severely deranged coagulation compared with a group with normal coagulation. We conclude that samples from arterial lines provide valid activated partial thromboplastin time results using a discard volume of either 4.5 ml or 16 ml.

Adult↗
PubMed1987

Prophylactic immunization against experimental leishmaniasis. VI. Comparison of protective and disease-promoting T cells.

In previous studies, we reported that mice immunized i.v. with lethally irradiated Leishmania major promastigotes developed substantial resistance to a subsequent L. major infection. However, such protection could be totally suppressed by prior s.c. injection with the same antigens. Both the protective immunity and the inhibition of its induction could be adoptively transferred with specific Lyt-2- T cells. Here, we present evidence showing that protection and disease promotion resulting from i.v. or s.c. immunization, respectively, are mediated by functionally distinct subsets of T cells. In a series of titration experiments, it was found that freshly isolated T cells derived from prophylactically i.v. immunized BALB/c mice were either protective (greater than 10(7) cells/recipient) or ineffective (less than 10(7) cells/recipient). No exacerbation of disease was observed at any dose. Conversely, T cells from mice immunized s.c. either accelerated disease development and inhibited protective immunization (greater than 10(7) cells/recipient) or had no effect (less than 10(7) cells/recipient). No protection was observed at any dose tested. In mixed transfer experiments, increasing numbers of T cells from s.c. immunized donors progressively inhibited the protective effect of T cells from i.v. immunized donors. Supernatant of T cell cultures from protectively immunized donors contained substantial macrophage-activating factor whereas such activity was not detectable in the supernatant of T cell culture from s.c. immunized donors. Analysis by flow cytometry showed that the spleen and lymph nodes of normal, i.v., or s.c. immunized BALB/c mice contained similar ratios of L3T4+ cells and Lyt-2+ cells.

Animals↗
PubMed1987

Is there an interleukin 2 inhibitor in human serum?

Normal mouse serum has been shown to contain an inhibitor of interleukin 2 (IL-2). Here we report that a molecule with similar activity cannot be found in normal human serum (NHS). Although NHS inhibited the IL-2-dependent proliferation of mouse CTLL cells, as expected of an IL-2 inhibitor, it also had inhibitory activity on IL-3-dependent cells and was cytolytic to IL-2-independent mouse cells as measured by a 51Cr release assay, indicating a nonspecific effect. In addition, NHS had no effect on the IL-2-dependent proliferation of human peripheral blood T-cell blasts. Fractionation of NHS by size exclusion HPLC failed to separate cytolytic activity from any putative true IL-2 inhibitor activity. The cytolytic component was not related to immunoglobulin since it had a molecular weight of 50,000 to 60,000 and was not bound by protein-A-Sepharose. However, its molecular weight, heat lability, and trypsin sensitivity suggest it to be a protein.

Blood Proteins↗